Salicylic Acid-Mediated Abiotic Stress Tolerance - Salicylic Acid: Plant Growth and Development - page 217

Two protein kinases with molecular masses of 48 and 40 kD are activated in
tobacco cells exposed to NaCl (Hoyos and Zhang 2000 ). The 48-kD protein kinase
was identified as SIPK. The activation of the 40-kD protein kinase is rapid and
dose-dependent. Other osmolytes such as Pro and sorbitol activate these two
kinases with similar kinetics. The activation of 40-kD protein kinase is specific for
hyperosmotic stress, as hypotonic stress does not activate it. Therefore, this 40-kD
kinase was named HOSAK (high osmotic stress-activated kinase). HOSAK is a
Ca 2+ -independent kinase. It has been also established that SIPK and 40-kD HO-
SAK are both components of a Ca 2+ - and ABA-independent pathway that may
lead to plant adaptation to hyperosmotic stress.
It was found that the UV-C-induced activation of SIPK was ROS-dependent,
since free radical scavengers completely abolished the activation of MAPK by
UV-C radiation in tobacco cell-suspension cultures (Miles et al. 2002 ), while the
activation of AtMPK6, the Arabidopsis homologue of SIPK, required both ROS
and Ca 2+ -influx (Miles et al. 2004 ). Cd treatment activated both MPK3 and MPK6
through the accumulation of ROS (Liu et al. 2010 ).
As shown in tobacco plants, ozone may also induce the rapid activation of SIPK
(Samuel and Ellisoverexpression lines 2002 ). Transgenic manipulation previously
showed that the overexpression of SIPK leads to enhanced ozone-induced lesion
formation with the concomitant accumulation of ROS. Ozone treatment strongly
induced ethylene formation in sensitive SIPK-overexpressing plants at ozone con-
centrations that failed to elicit stress ethylene release in wild-type plants. By con-
trast, SIPK-overexpressing plants displayed no ozone-induced SA accumulation,
whereas wild-type plants accumulated SA upon ozone exposure. The epistatic
analysis of SIPK-overexpressing function suggests that the ozone-induced cell death
observed in SIPK-overexpressing plants is either independent, or upstream, of SA
accumulation (Samuel et al. 2005 ). The initial activation of AtMPK6 and AtMPK3
by ozone in Arabidopsis was also independent or upstream of SA, ethylene or JA
signalling, since the activation pattern was similar in mutants deficient for the
respective cascades. However, hormones are intertwined with MAPKs, since the
activation of AtMPK6 was prolonged and AtMPK3 activation delayed in the eth-
ylene-insensitive etr1 mutant. Additionally, the basal expression level of AtMPK3
was only half the wild-type levels in SA-insensitive and -deficient accessions, and
this lower level of expression was also reflected in AtMPK3 activity (Ahlfors et al.
2004 ). AtMPK6/SIPK and AtMPK3/WIPK are induced, among other stresses, by
ozone, and are also activated by H 2 O 2 and superoxide. Although both AtMPK6 and
AtMPK3 are rapidly activated by ozone, the regulation of their activity by ozone is
different. AtMPK3 was up-regulated by ozone at the transcriptional, translational
and on post-translational levels, whereas only the post-translational activation of
kinase activity was detected for AtMPK6. In addition, the activation of AtMPK3
lasted longer than that of AtMPK6. Plant ozone sensitivity and the expression of
antioxidant genes is affected by these kinase classes, since both suppression and
overexpression of the tobacco SIPK led to increased ozone sensitivity and changes in
the expression of APX and GST (Kangasjärvi et al. 2005 ). In ozone-stressed
transgenic plants of tobacco SIPK seems to regulate the activity of WIPK (the